Wnt signaling is known to control numerous cellular processes during embryogenesis, including the directed rearrangement of cells during morphogenetic movements such as convergent extension. The intercalation of dorsal hypodermal (epidermal) cells during morphogenesis in C. elegans is arguably one of the simplest cases of such directed rearrangement. Based on laser killing experiments, dorsal intercalation occurs autonomously among exceedingly small cohorts of dorsal hypodermal cells, suggesting polarizing events act very locally within the hypodermis. We show here that Wnt signaling components act as developmental regulators of these local processes. Embryos from
dsh-2(
or302)/Dishevelled mothers have defects at all stages of hypodermal morphogenesis. During dorsal intercalation, cells often fail to migrate or intercalate properly.
or302 embryos often display defects in migration during the concurrent ventral enclosure of the hypodermis, resulting in failure of hypodermal sheet sealing at the ventral midline, and subsequent rupture. In addition, seam cells often display an invasive cell behavior, migrating into the dorsal or ventral arrays of hypodermal cells. A structure-function analysis of
dsh-2 reveals that all three of its major domains (DIX, PDZ and DEP) are necessary for its function. Surprisingly, removal of the function of homologues of known planar cell polarity (PCP) effectors does not result in defects in morphogenesis, suggesting that if a PCP-like pathway operates in C. elegans, it may use novel effectors to control cell movements. In contrast, we show that Wnt/β-catenin signaling, through WRM-1/β-catenin and LIT-1/NLK, acts during mid-embryogenesis, several cell divisions prior to terminal divisions in the hypodermis, to affect hypodermal morphogenesis. The POP-1/Tcf co-activator, SYS-1, is also involved in these events. These results suggest that Wnt signaling acts during patterning of the hypodermis, and possibly later, to influence cell rearrangement events.